Diffusion-weighted MRI in transient global amnesia: Introduction

Citation
M. Strupp et al., Diffusion-weighted MRI in transient global amnesia: Introduction, KLIN NEUROP, 31, 2000, pp. S18-S22
Citations number
35
Categorie Soggetti
Neurology
Journal title
KLINISCHE NEUROPHYSIOLOGIE
ISSN journal
14340275 → ACNP
Volume
31
Year of publication
2000
Supplement
1
Pages
S18 - S22
Database
ISI
SICI code
1434-0275(200005)31:<S18:DMITGA>2.0.ZU;2-R
Abstract
Transient global amnesia (TCA) represents a transient benign self-limiting cerebral dysfunction of unknown aetiology. It manifests as a sudden failure of anterograde and retrograde memory lasting for several hours and subsidi ng gradually. Prompted by the findings of previous positron emission tomogr aphy and single-photon emission computed tomography studies demonstrating h ypo- or hyperperfusion in the left temporal lobe in isolated patients with TGA, we compared the sensitivity of diffusion-weighted magnetic resonance i maging (DWI) with that of conventional T-1-/T-2-weighted MRI in patients wi th TGA. Methods: Fifteen patients with the typical syndrome of a pure TCA w ere included in the study. For all patients a coronal DWI gradient echo seq uence ("steady-state free precession [SSFP] sequence") and conventional T-1 -/T-2-weighted turbo spin-echo sequences were obtained. In addition, 5 pati ents were also examined by echo-planar imaging (EPI) sequence. Results: Ele ven of the 15 patients had elevated signal intensity in the left hippocampa l region in the DWI-SSFP; moreover, 5 of these 12 patients exhibited bilate ral signal abnormality in this sequence. All conventional T-1-/T-2-weighted images as well as all follow-up studies were normal. No signal changes wer e observed in the EPI sequences, but there were artifacts at the skull base in all of them, which made it difficult to evaluate the images. Discussion : The signal elevation in DWI correlates with a decrease in the interstitia l space and cellular oedema in the temporal robe during TCA. The underlying pathomechanism causing this cellular oedema cannot be clearly outlined usi ng DWI. Our data are compatible with spreading depression, but do not prove it. It remained unclear why there were only changes in the SSFP, but not i n the EPI sequences.